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通过不同辐射质量的低剂量照射增强非恶性和恶性细胞中过氧化物酶的释放

Enhancement of Peroxidase Release from Non-Malignant and Malignant Cells through Low-Dose Irradiation with Different Radiation Quality.

作者信息

Abdelrazzak Abdelrazek B, Pottgießer Stefanie J, Hill Mark A, O'Neill Peter, Bauer Georg

机构信息

a  CRUK/MRC Oxford Institute for Radiation Oncology, University of Oxford, Oxford OX3 7DQ, United Kingdom; and.

b  Institute of Virology, Department of Medical Microbiology and Hygiene, University Medical Center, Freiburg, Germany.

出版信息

Radiat Res. 2016 Feb;185(2):199-213. doi: 10.1667/RR14245.1. Epub 2016 Feb 5.

Abstract

The release of peroxidase by nontransformed or transformed fibroblasts or epithelial cells (effector cells) triggers apoptosis induction selectively in transformed fibroblasts or transformed epithelial cells (target cells) through intercellular apoptosis-inducing signaling. The release of peroxidase can be induced either by treatment with transforming growth factor beta 1 or by low doses of alpha particles, gamma rays or ultrasoft X rays. In addiation, data indicates that radiation quality does not determine the overall efficiency of peroxidase release and the effects among a wide range of radiation doses are indistinguishable. These findings suggested that peroxidase release might be being triggered through intercellular bystander signaling. We show here that maximal peroxidase release does indeed occur after coculture of a small number of irradiated cells with an excess of unirradiated cells and demonstrate an enhanced effector function of nontransformed cells after the addition of a small number of irradiated cells. These data strongly indicate that peroxidase release is indeed triggered through bystander signaling mechanisms in mammalian cells.

摘要

未转化或转化的成纤维细胞或上皮细胞(效应细胞)释放的过氧化物酶,通过细胞间凋亡诱导信号传导,选择性地触发转化的成纤维细胞或转化的上皮细胞(靶细胞)中的凋亡诱导。过氧化物酶的释放可通过用转化生长因子β1处理或低剂量的α粒子、γ射线或极软X射线诱导。此外,数据表明辐射质量并不决定过氧化物酶释放的总体效率,并且在广泛的辐射剂量范围内的效应是无法区分的。这些发现表明过氧化物酶释放可能是通过细胞间旁观者信号传导触发的。我们在此表明,在少量受辐照细胞与过量未受辐照细胞共培养后,确实会发生最大程度的过氧化物酶释放,并证明在添加少量受辐照细胞后未转化细胞的效应功能增强。这些数据有力地表明,过氧化物酶释放确实是通过哺乳动物细胞中的旁观者信号传导机制触发的。

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